The study investigates the K210del mutation in genetic cardiomyopathy, which impairs myocardial contractility due to calcium discoordination in the troponin complex.

Using a structure-based drug repurposing approach, researchers identified risedronate, an FDA-approved bisphosphonate, as a structural corrector that restores the calcium-binding domain's normal configuration.

Experiments with patient-derived iPSC cardiomyocytes and a mouse model demonstrated that risedronate normalized calcium sensitivity, improved contraction velocity, and restored left ventricular function.

The findings highlight the potential of repurposing existing drugs to treat genetic cardiomyopathies.